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目的探讨一氧化氮（ＮＯ）在急性肝坏死大鼠模型中的浓度动态变化及其可能的作用机制．方法通过用化学药物促进或抑制急性肝坏死大鼠ＮＯ的合成，检测其外周血ＮＯ及ＡＬＴ，ＡＳＴ的浓度变化，并观察肝脏的病理变化．结果①急性肝坏死大鼠血清ＮＯ浓度６，１２，２４，４８ｈ显著高于正常对照（μｍｏｌ／Ｌ，９０±１３，１３７±３１，６６±１６，４４±１０ｖｓ１６±６，分别为Ｐ＜００１，Ｐ＜００１，Ｐ＜００１，Ｐ＜００５）；ＡＬＴ，ＡＳＴ也显著升高（ＡＬＴ，Ｕ／Ｌ，６９８±１０８，２０５６±６６８，８５８±２０８，１９６±３４ｖｓ３５±１３，Ｐ＜００１；ＡＳＴ，Ｕ／Ｌ，８０１±９４，３５７５±７１４，１２７２±２４２，１７５±１２７ｖｓ６５±２２，Ｐ＜００１）；②用ＮＡＭＥ抑制ＮＯ合成，降低了急性肝坏死大鼠外周血ＮＯ浓度，却显著升高了ＡＬＴ，ＡＳＴ浓度．③急性肝坏死大鼠应用ＮＯ合成底物后，与阳性对照组相比，未见ＮＯ显著升高，ＡＬＴ，ＡＳＴ也无显著变化．结论ＮＯ对ＤＧａｌｎ／ＬＰＳ诱导的急性肝坏死大鼠肝组织具有保护作用．
Objective To investigate the dynamic changes of nitric oxide (NO) concentration in rat model of acute hepatic necrosis and its possible mechanism. Methods By using chemical drugs to promote or inhibit the synthesis of NO in rats with acute hepatic necrosis, the concentrations of NO, ALT and AST in peripheral blood were measured and the pathological changes of liver were observed. Results ① The levels of NO in serum of acute hepatic necrosis rats were significantly higher than those of normal controls (μmol / L, 90 ± 13,137 ± 31,66 ± 16,44 ± 10 vs16 ± 6, P <0 01, P <001, P <001, P <005); ALT, AST were also significantly increased (ALT, U / L, 698 ± 108, 2056 ± 668, 858 ± 208, 196 ± 34vs35 ± 13, P <001; AST, U / L, 801 ± 94,3575 ± 714,1272 ± 242,175 ± 127vs65 ± 22, P <001); ② NAME inhibited NO synthesis and decreased Acute liver necrosis in rats with peripheral blood NO concentration, but significantly increased ALT, AST concentration. ③No significant increase of NO and ALT, AST were observed in acute liver necrosis rats after application of NO synthesis substrate compared with the positive control group. Conclusion NO has a protective effect on hepatic tissue induced by DGaln / LPS in rats with acute hepatic necrosis.